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Flashcards in W3 : Deck (55):
1

what are the effects of stimulation of å1 adrenoceptor?

the site is at blood vessels ; can be used for shock

agonist does the following :
1. increase peripheral resistance
2. increase BP
3. mydriasis
4. increase closure of internal sphincter of bladder

2

what are the effects of stimulation of ß1 adrenoceptor?

agonist does the following :
1. tachycardia
2. increase lipolysis
3. increased myocardial contractility
4. increase release of renin

can be used for HT failure

3

what are the effects of stimulation of ß2 adrenoceptor?

agonist does the following :
1. vasodilation
2. slightly decrease peripheral resistance
3. bronchodilation
4. increase muscle and liver glycogenolysis
5. increase release of glucagon
6. relax uterine smooth muscle (can prevent preterm delivery)

4

what are DIRECT acting adrenergic agonist?

these drugs act directly on å or ß receptors, producing effects similar to those that occur following stimulation of sympathetic nerves or release the hormone epinephrine from the adrenal medulla

there are two types of DIRECT acting adrenergic agonist :
1. catecholemines
2. noncatecholemines

5

epinephrine

direct acting adrenergic agonist
catecholemines

å1, å2, ß1, ß2
used in intense asthma
anaphylactic shock, etc.

6

dobutamine

direct acting adrenergic agonist
catecholemines

ß1
drug of choice to stimulate heart

7

dopamine

direct acting adrenergic agonist
catecholemines

å1, ß1
used to treat shock

8

phenylephrine

direct acting adrenergic agonist
noncatecholemines

å1
causes intense vasoconstriction

9

terbutaline

direct acting adrenergic agonist
noncatecholemines

ß2
used as bronchodilator (asthma)

10

albuterol

direct acting adrenergic agonist
noncatecholemines

ß2
used as bronchodilator (asthma)

11

salmeterol

direct acting adrenergic agonist
noncatecholemines

ß2
long acting bronchodilator

12

what are INDIRECT acting adrenergic agonist?

they cause norepinephrine release from presynaptic terminals or inhibit the uptake of nor-epinephrine

13

amphetamine

INDIRECT acting adrenergic agonist

has CNS stimulatory effects
used for narcolepsy, ADHD, appetite control

14

methylphenidate

same as amphetamine

INDIRECT acting adrenergic agonist
has CNS stimulatory effects
used for narcolepsy, ADHD, appetite control

15

what happens if a patient taking MAO-inhibitors eat lots of cheese?

1. tyraminine is oxidized by MAO (manoamine oxidase)
2. if patient taking MAP-inhibitors eat cheese, tyramine of cheese cannot be oxidized
3. tyramine enters nerve terminal, and displaces store norepinephrine, thereby causing hypertensive crisis

[patient can carry 25mg tablets of chlorpromazine for emergency]

16

what are adrenergic antagonist?

these drugs bind to the adrenergic receptors and PREVENT their activation by endogenous epinephrine and norepinephrine

there are :
1. å-adrenergic blocking agents (non-selective & selective)
2. ß-adrenergic blocking agents (non-selective & selective)
3. å & ß blockers

17

what are 2 families of adrenergic receptors?
and how are they further subdivided?

å adrenoceptor & ß adrenoceptor

å adrenoceptor are subdivided into two groups :

å 1 and å 2 - these are further subdivided into :
å 1A, å 1B, å 1C, å 1D & å 2A, å 2B, å 2C

18

MOA of non-selective å blocker (å1 and å2 blockers)?

there drugs block both å adrenergic receptors causing vasodilation and lowering blood pressure

19

Phenoxybenzamine

adrenergic antagonist(å1 and å2 blockers)

cause vasodilation and lower blood pressure

tx of pheochromocytoma (tumor of adrenal medulla, which produces too much epinephrine),
tx of hypertensive episodes

20

doxazosin

adrenergic antagonist
selective å1 blocker

tx. hypertension (can cause orthostatic hypotension

21

tamsulosin

adrenergic antagonist
selective å1A blocker

relaxes smooth muscle in urinary bladder neck and prostate--> improving urine flow in benign prostate hyperplasia

22

clonidine

adrenergic antagonist
å2 agonist (in blood vessel)

inhibits both sympathetic output from the brain and release of norepinephrine from nerve terminals--> reduce blood pressure

tx. hypertension

23

MOA of ß-adrenergic blocking agents?

all the clinically available ß-blockers are competitive antagonist

non-selective ß-blockers act at both ß1 and ß2 receptors, whereas cardioselective ß-antagonists primarily block ß2 receptors

24

propranolol

ß-adrenergic blocking agent (all tx Hypertension)

*tx. angima, cardia arrhythmias, myocardial infarction, congestive heart failure, hyperthyroidism, and glaucoma as well as serving in the prophylaxis of migraine HA

ci. ASTHMA

25

sotalol

ß-adrenergic blocking agent (all tx Hypertension)

*used for ventricular arrhythmias and tachycardia

ci. ASTHMA

26

metoprolol

ß1 - selective blocker

tx. hypertension, myocardial infarction, agina pectoris

27

atenolol

ß1 - selective blocker

28

which drugs are mixed å and ß blockers?
and their actions?

labetalol - å1, ß1, ß2 blockers (used for pre-eclampsia)
carvedilol - å1, ß1, ß2 blockers

ax. decrease BP wo reflec tachycardia
tx. hypertension

29

what are cautions needed to take when a patient w type 1 diabetes is to be given Propranolol, and why?

ß blocker leads to decreased glycogenolysis and decreased glucagon secretion.

Thus, very careful monitoring of blood glucose is essential bc pronounced hypoglycemia may occur after insulin injection. also reflex increase in HT rate that occurs in response to hypoglycemia is also blocked by ß-blockers

30

what are risks of withdrawing ß blockers? how can this be avoided?

tx w ß blockers when stopped abruptly risks severe precipitating cardiac arrhythmias.

the ß blockers must be tapered off gradually for at least a few weeks. Long term tx w ß antagonist leads to up-regulation of the ß receptors.

on suspension of therapy, the increased receptors can worsen angina or hypertension.

31

name excitatory and inhibitory neurotransmitters of brain?

excitatory neurotransmitters of CNS : acetylcholine, norepinephrine, dopamine, serotonin

inhibitory neurotransmitters of CNS : GABA, glycine

32

what are 3 types of anti-Parkinson drugs?

1. dopamine replacement therapy
2. dopamine receptor agonist therapy - AD agonists can be sued be although dopamine-releasing neurons have disappeared, the postsynaptic dopamine receptors are still present and functional. Administration of dopamine agonists to stimulate these receptors should therefore restore balance of inhibition and excitation in basal ganglia

3. anticholinergic therapy - muscarinic antagonists used in Parkinson's disease. they reduce Ach:Dopamine imbalance in striatum. side effects of these drugs include dry mouth, constipation, urinary retention, confusion.

33

what is etiology of Parkinson's disease?

loss of dopamine-containing neurons that project from substantial nigra to striatum where they inhibit cholinergic (AcH) neurons.

Normally, striatum is connected to the substantial nigra by neurons that secrete the inhibitory transmitter GABA at their termini in substantia nigra.

In turn, substantial nigra sends neurons back to the striatum, secreting transmitter dopamine at their termini. This mutual inhibitory pathway normally maintains a balance. Destruction of cells of substantial nigra results in overproduction of Acetylcholine which triggers a chain of abnormal signaling, resulting in loss of control of muscle movement.

34

levodopa

1. dopamine replacement therapy

metabolic precursor of dopamine
decarboxylated to dopamine in brain. DA does not cross blood-brain barrier

35

carbidopa

1. dopamine replacement therapy

diminishes decarboxylation of levodopa (L-dopa) in peripheral tissues thereby prevent sits peripheral biotransformation

36

sinemet

1. dopamine replacement therapy

combination of levodopa and carbidopa

37

selegiline

1. dopamine replacement therapy aka deprenyl

inhibitor of monoamine oxidase_B (MOA-B), the enzyme that metabolizes dopamine in CNA

38

amantidine

1. dopamine replacement therapy

antiviral drug effective in tx of influenza
also, enhances synthesis, release or reputed of dopamine from surviving neurons

39

what two drugs are used in dopamine receptor agonist therapy?

ropinirole & bromocriptione (powerful dopamine-receptor agonist)

40

etiology of Alzheimer Disease (AD)?

1. formation of Beta-amyloid plaque
2. neurofibruatory tangles

decrease in choline acetyltransferase (that catalyzes the transfer of acetyl group of acetyl CoA to choline, forming acetylcholine) and other markers of cholinergic neuron activity.

Eventually, cholinergic neurons die or are destroyed.

tx. focused on increasing amount of acetylcholine in synapse by inhibiting the breakdown of acetylcholine.

the most recent drug is an antagonist of N-methyl_Dasparate (NMDA) receptor (Glutamate receptor). Overstimulation of these receptors may be a mechanism of neurodegenrative process in AD.

41

donezepil

anti-alzheimer drug
cholinesterase inhibitor

42

memantine

anti-alzhiemer drug
NMDA antagonist
*antagonist of N-methyl-D-asparate (NMDA) receptor (Glutamate receptor). Overstimulation of these receptors may be a mechanism of neurodegenerative process in AD

appears to slow the progression of AD (slows the rate of memory loss)

43

what are Anxiolytic and Hypnotic drugs?
what are the 3 types?

tx. anxiety, epilepsy, sleep induction, and anesthesia, etc.
often called sedative-hypnotics or just anxiolytics.

cross tolerance occurs btw all the CNS sedative including the barbiturates, benzodiazepines (BZDs), and ethanol

1. barbiturates
2. benzodiazepines
3. other

44

MOA of Barbiturates?

enhance the fx of y-aminobutyric acid (GABA) in CNS by enhancing the duration of chloride channel openings. this ax. hyper-polarizes the cell, and causes an increase in inhibition of CNS.

1. produces sedation at low doses ; at high doses, can cause hypnosis, coma, death
2. induce LV P-450 yste, so metabolism of other drugs will be altered in its presence
3. physical deepness occurs after chronic use

*selection of particular barbiturate depends on duration of ax of agent, which in turn depends on its lipid solubility

45

what are withdrawal sx of barbiturates?

anxiety, nausea, vomiting, hypotension, seizures and psychosis
CV collapse may develop leading to death

46

phenobarbital

anxiolytic and hypnotic drug
long acting barbiturate (1-2 days)
used as anticonvulsant in epilepsy

47

amobarbital

anxiolytic and hypnotic drug
short acting barbiturate (3-8 hours)
used in anesthesia

48

MOA & ax of benzodiazepines

difference btwn barbiturates and benzodiazepines?

used most widely as anxiolytic drug

MOA : bind to specific site on Nueronal GABA receptors. this binding enhances the affinity of GABA receptors for GABA, resulting in more frequent opening of chloride channels. the increase chloride cases increased inhibition.

ax. : all BZD reduce anxiety and cause sedation

difference : unlike barbiturates, BZD reduce anxiety at does that do not produce sedation. some agents are used as anti-epileptic agents and some are used in induction of anesthesia. duration of ax and pharmacokinetic properties are important considerations in selecting drugs to be used.

49

dependence and withdrawal sx of benzodiazepines?

physical and psychological dependence of BZD can occur.

withdrawal : confusion, anxiety, agitation, restlessness

BZD with short half-life induce more abrupt and severe withdrawal reactions than do drugs w longer half-lives

50

diazepam (valium)

anxiolytic and hypnotic drug
long acting benzodiazepines

used for anxiety disorders, skeletal muscle spasm, spasticity from degenerative disorders such as MS and cerebral palsy

51

alprazolam

anxiolytic and hypnotic drug
long acting benzodiazepines

used as antidepressant, anxiolytic
tx of panic attacks

52

oxazepam

anxiolytic and hypnotic drug
long acting anxiolytic and hypnotic drug

useful for tx elderly patients and patients w liver dysfunction bc it does not rely on LV for metabolism

53

which benzodiazepines are used in tx of status epileptics and alcoholic withdrawal?

tx of stars epileptics : diazepam and lorazepam

alcoholic withdrawal : chlordiazepoxide

54

what are the advantages of using ZOLPIDEM?
what effect of this drug has been seen on vegetative state of patient?

anxiolytic drug

used for short term tx of insomnia, show no tolerance or withdrawal effects.

it is said to WAKE persistent vegetative state with brain injuries

55

MOA and use of flumazenil?

anxiolytic and hypnotic drug
a competitive benzodiazepines receptro antagonist

can be used to reverse the sedative effects of benzodiazepines after anesthesia or after overdose with BZD